期刊
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
卷 174, 期 -, 页码 690-698出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2019.03.028
关键词
COFs-derived PM2.5; HUVECs; NLRP3; VEGF; Tube formation
资金
- National Natural Science Foundation of China [81872580]
- Natural Science Foundation of Anhui Province [1708085MH220]
- Anhui Province Science and Technology Innovation Project Demonstration Project [201707d08050003]
- Foundation of Natural Science for Colleges and Universities in Anhui Province [KJ2018A0167]
- Project Foundation for the Young Talents in Colleges of Anhui Province [gxyq2017003]
- Grant for Scientific Research of BSKY from Anhui Medical University [XJ201621]
- Student's Platform for Innovation and Entrepreneurship Training Program of China [201810366031]
Background: Cooking oil fumes (COFs), a main pollutant in kitchen air, is a major risk to human health. In our previous research, exposure to COFs-derived PM2.5 could cause umbilical vascular endothelial dysfunction, leading to decreased fetal weight. Here, to test the role of ROS-mediated NLRP3 inflammasome pathway in blood vessel formation of human umbilical vein endothelial cells (HUVECs) caused by COFs-derived PM2.5, the cells were exposed to COFs-derived PM2.5 at different concentrations with and without N-acetyl-L-cysteine (NAC). Methods: MTT assay was used to determine HUVECs viability. Intracellular ROS and mitochondrial ROS levels were assessed with DCFH-DA and MitoSOX (TM) assay. The levels of proteins and mRNA involved in NLRP3 inflammasome signaling pathway and VEGF were measured by western blot and real-time PCR (RT-PCR). Tube formation in HUVECs was detected by tube formation assay. Results: The results revealed that COFs-derived PM2.5 exposure reduced HUVECs viability, increased the intracellular and mitochondrial ROS levels in cells, and up-regulated the levels of proteins and mRNA involved in NLRP3 inflammasome signaling pathway. However, the protein and mRNA expression of VEGF were reduced with the increasing exposure concentrations. In addition, COFs-derived PM2.5 also affected the tube formation. However, co-incubation with NAC effectively rescued the damages caused by COFs-derived PM2.5 exposure. Conclusions: This study proved that COFs-derived PM2.5 could significantly reduce HUVECs viability, induce the overproduction of ROS, lead to inflammation and inhibit VEGF expression, thus affect angiogenesis of HUVECs in vitro. It was revealed that the impact caused by COFs-derived PM2.5 on blood vessel formation through a ROS-mediated NLRP3 inflammasome pathway.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据